<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>1405-888X</journal-id>
<journal-title><![CDATA[TIP. Revista especializada en ciencias químico-biológicas]]></journal-title>
<abbrev-journal-title><![CDATA[TIP]]></abbrev-journal-title>
<issn>1405-888X</issn>
<publisher>
<publisher-name><![CDATA[Universidad Nacional Autónoma de México, Facultad de Estudios Superiores Zaragoza]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1405-888X2023000100213</article-id>
<article-id pub-id-type="doi">10.22201/fesz.23958723e.2023.597</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Acciones del peróxido de hidrógeno (H2O2) como señalizador redox y como agente de estrés oxidante en la diabetes mellitus]]></article-title>
<article-title xml:lang="en"><![CDATA[Role of hydrogen peroxide (H2O2) as a redox signaling molecule and in the diabetes mellitus-related oxidative stress]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ulloa]]></surname>
<given-names><![CDATA[Miriam]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Macías]]></surname>
<given-names><![CDATA[Fernando]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Martínez de la Escalera]]></surname>
<given-names><![CDATA[Gonzalo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Arnold]]></surname>
<given-names><![CDATA[Edith]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Nacional Autónoma de México Instituto de Neurobiología Departamento de Neurobiología Celular y Molecular]]></institution>
<addr-line><![CDATA[Querétaro Querétaro]]></addr-line>
<country>México</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Universidad Nacional Autónoma de México Instituto de Neurobiología ]]></institution>
<addr-line><![CDATA[Querétaro Querétaro]]></addr-line>
<country>México</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>00</month>
<year>2023</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>00</month>
<year>2023</year>
</pub-date>
<volume>26</volume>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S1405-888X2023000100213&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S1405-888X2023000100213&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S1405-888X2023000100213&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen En las reacciones bioquímicas del metabolismo donde participa el oxígeno molecular se presenta una constante formación de especies reactivas de oxígeno (ROS). Entre las diferentes ROS, destaca el peróxido de hidrógeno (H2O2) por su papel en la fisiología celular, ya que participa como segundo mensajero en múltiples procesos celulares como la proliferación celular, la síntesis y la secreción de hormonas, la regulación y la activación de células inmunes, la angiogénesis y los procesos apoptóticos. Sin embargo, un aumento exacerbado en la formación y la acumulación de H2O2, producido por el incremento en la actividad de la cadena transportadora de electrones en la mitocondria, la autooxidación de la glucosa y/o la activación de la vía del sorbitol, genera un desequilibrio en el estado de óxido-reducción de las células. Esta acumulación de H2O2 puede causar un daño celular a través de la oxidación de las proteínas, los lípidos, los carbohidratos y los ácidos nucleicos; al contribuir en el desarrollo y la progresión de enfermedades degenerativas y metabólicas como la diabetes mellitus. Al subir la concentración de la glucosa en la sangre, se presenta un incremento en la concentración del H2O2, que intensifica los procesos oxidantes que están ligados a la patogénesis, la progresión y las complicaciones de la diabetes mellitus.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Cellular metabolism is a constant source of reactive oxygen species (ROS). The production of hydrogen peroxide (H2O2) is particularly relevant, due to its role in cellular physiology. H2O2 can act as a classical intracellular signaling molecule in several processes like cell proliferation, hormone synthesis and secretion, immune cell regulation, angiogenesis, and apoptosis. However, H2O2 overproduction and accumulation, derived from increased mitochondrial electron transport chain activity, glucose autoxidation, and increased polyol flux, contribute to an imbalance in the redox state of the cells. High concentration of H2O2 induces cellular dysfunction through oxidation of macromolecules like proteins, lipids, carbohydrates and nucleic acids. H2O2-induced oxidative damage can contribute to the development and progression of degenerative diseases such as diabetes mellitus. Indeed, chronic hyperglycemia has been shown to cause an increased H2O2 concentration and oxidative damage that contribute to the pathogenesis and progression of diabetes complications.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[peróxido de hidrógeno]]></kwd>
<kwd lng="es"><![CDATA[especies reactivas del oxígeno]]></kwd>
<kwd lng="es"><![CDATA[señalización redox]]></kwd>
<kwd lng="es"><![CDATA[diabetes]]></kwd>
<kwd lng="es"><![CDATA[estrés oxidante]]></kwd>
<kwd lng="en"><![CDATA[hydrogen peroxide]]></kwd>
<kwd lng="en"><![CDATA[reactive oxygen species]]></kwd>
<kwd lng="en"><![CDATA[redox signaling]]></kwd>
<kwd lng="en"><![CDATA[Diabetes]]></kwd>
<kwd lng="en"><![CDATA[oxidative stress]]></kwd>
</kwd-group>
</article-meta>
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